Ulcerative colitis (UC) has become a global health issue. This study evaluated whether administering Lactiplantibacillus plantarum CGMCC9513 to dextran sulfate sodium (DSS)-induced colitis mice could alleviate colitis by modulating gut microbiota imbalance and activating the aryl hydrocarbon receptor (AhR) to enhance intestinal barrier function. The anti-inflammatory effect and AhR activation ability of L. plantarum CGMCC9513 were evaluated with lipopolysaccharide (LPS)-induced cell inflammation model; 25 male BALB/c mice were divided into blank group (CNG), model group (DSS), L. plantarum CGMCC9513-treated group (LPDT), and L. plantarum CGMCC9513 control group (LP). The mice were pre-administered L. plantarum CGMCC9513 for 14 days and continued to receive it during DSS induction. Symptoms during induction, goblet cell count, expression of MUC2 and Occludin proteins, and changes in gut microbiota were observed. Subsequently, the expression of cytokines interleukin-10 (IL-10), tumor necrosis factor (TNF-α), interleukin-1β (IL-1β) and AhR activation status was determined. The study found that L. plantarum CGMCC9513 could alleviate cell inflammation induced by LPS and activate AhR in vitro. For colitis mice, it could reduce colonic mucosal damage and enhance intestinal barrier function. Regarding gut microbiota changes, L. plantarum CGMCC9513 mainly downregulated Bacteroides, Blautia, Escherichia-Shigella, and Lachnospiraceae_ NK4A136_group and upregulated Firmicutes, Lactobacillus. It reduces the risk of bacterial translocation and increases beneficial gut bacteria. L. plantarum CGMCC9513 reduced the expression of pro-inflammatory cytokines TNF-α and IL-1β while increasing the expression of anti-inflammatory cytokine IL-10. Meanwhile, increased expression of AhR and Cytochrome P450 1A1 (CYP1A1) proteins indicated AhR activation by L. plantarum CGMCC9513. In conclusion, L. plantarum CGMCC9513 can synergistically enhance intestinal barrier alleviation in colitis mice by modulating gut microbiota imbalance and activating AhR.